Home / Resources / Clinical Gems / Practical Diabetes Care, 3rd Ed., Excerpt #20: Diabetes and the Eye Part 4 of 4

Practical Diabetes Care, 3rd Ed., Excerpt #20: Diabetes and the Eye Part 4 of 4

May 25, 2015

David Levy, MD, FRCP     


Diabetes is a strong risk factor for cataract, and it occurs earlier and progresses faster than in the non-diabetic population. Cortical cataract is the most frequent, with its typical radial spoke opacities. Indications for cataract surgery include impairment of vision that reduces quality of life, and suspicion of retinopathy or other retinal or optic nerve pathology obscured by cataract.


Cataract surgery in diabetes is more difficult and carries worse visual outcomes. Complications are more frequent, for example rapid progression of retinopathy, posterior capsule opacification, iris neovascularization and, very rarely, endophthalmitis, but results are continually improving. Systemic a-adrenergic blocking drugs for hypertension, often used in diabetes, are associated with the rare intraoperative floppy iris syndrome. The optimum timing of laser treatment in relation to cataract surgery is still debated [9]….

Retinal vascular occlusions
Occlusions of the retinal artery and vein (and their branches) are common. Atherosclerotic risk factors are, naturally, associated with arterial occlusion, and retinal artery occlusions are more common in diabetes, but the association with venous occlusions is less strong. Most patients will present to the ophthalmologist, but diabetes team input is important.

Retinal artery occlusions
Both central and branch retinal artery occlusions frequently result from microemboli from atherosclerotic plaques and calcified cardiac valves. They present with acute unilateral visual impairment. Importantly, the retina may appear normal, but is usually whitened and opacified (segmental if there has been a branch occlusion). The cherry-red spot is characteristic. Investigate a structural source with a carotid Doppler study and an echocardiogram. All vascular risk factors must be carefully managed, especially smoking. There are no specific ophthalmological treatments. Non-arteritic ischemic optic neuropathy causes painless visual loss through occlusion of the posterior ciliary artery supplying the optic nerve. It has been rarely associated with the phosphodiesterase (PDE)5 inhibitors used in the treatment of erectile dysfunction (see Chapter 10).

Retinal vein occlusions
These are more common than arterial occlusions, and again can be central or branch. They may not be primary events; a thickened atherosclerotic retinal artery overlying a vein at an arteriovenous crossing may disturb blood flow and cause thrombosis. The major risk factor is hypertension, but ocular hypertension and other vascular risk factors are important. The retinal appearance is characteristic and dramatic (‘tomato splash’), with widespread hemorrhages, and is sometimes mistaken for advanced retinopathy. Again, management of arterial risk factors is important, but investigate for a prothrombotic cause in patients with previous venous thromboembolic disease. Macular grid treatment is probably the best at present, but anti-VEGF treatments are being trialled, and a 6-month course of intravitreal bevacizumab may improve the visual outcome.

New developments
Several drugs are in development or in clinical trials that may retard progression of pre-proliferative retinopathy or maculopathy. The main interest is in maculopathy, which frequently does not respond to standard treatments. Ruboxistaurin, an orally active protein kinase C [3-isoform antagonist, has been in trials for several years. It does not seem to retard progression of retinopathy, but it slows progression of maculopathy and moderately severe to very severe non-proliferative retinopathy. Further trials are in progress. There is increasing interest in agents that bind or antagonize VEGF and which, given by intravitreal injection, are already in widespread use in neovascular AMD. These include the recombinant humanized monoclonal antibodies bevacizumab (Avastin) and its modification ranibizumab (Lucentis); small studies have given inconsistent results but, pending substantive RCTs, they are often used off-licence in macular oedema which is not responding to other treatments, and where the maculopathy is so close to the avascular zone that laser treatment is not possible. There is also interest in their use in proliferative retinopathy, and substantial trials are in progress. Pegaptanib, which binds VEGF, may also prove valuable, as may aflibercept, an inhibitor of VEGF receptor expression. There is concern that systemic absorption of these agents may carry a small risk of thromboembolism. Intravitreal glucocorticoids (e.g. triamcinolone) have been used in macular oedema, but are probably less effective than laser treatment. They tend to cause raised intraocular pressure, and late cataract formation is common.


  1. Nathan DM, Zinman B, Cleary PA et al. Modern-day clinical course of type 1 diabetes mellitus after 30 years’ duration: the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications and Pittsburgh epidemiology of diabetes complications experience (1983–2005). Arch Intern Med 2009;169:1307–16. PMID: 19636033.
  2. Hariprasad SM, Mieler WF, Grassi M, Green JL, Jager RD, Miller L. Vision-related quality of life in patients with diabetic macular oedema. Br J Ophthalmol 2008;92:89–92. PMID: 17584999.
  3. Beulens JW, Patel A, Vingerling JR et al. Effects of blood pressure lowering and intensive glucose control on the incidence and progression of retinopathy in patients with type 2 diabetes mellitus: a randomised controlled trial. Diabetologia 2009;52:2027–36. PMID: 19633827.
  4. Chew EY, Ambrosius WT, Davis MD et al. Effects of medical therapies on retinopathy progression in type 2 diabetes. ACCORD Study Group and ACCORD Eye Study Group. N Engl J Med 2010;363:233–44.
  5. Chaturvedi N, Porta M, Klein R et al. Effect of candesartan on prevention (DIRECT-Prevent 1) and progression (DIRECT-Protect 1) of retinopathy in type 1 diabetes: randomised, placebo-controlled trials. Lancet 2008;372:1394–402. PMID: 18823656.
  6. Sjølie AK, Klein R, Porta M et al. Effect of candesartan on progression and regression of retinopathy in type 2 diabetes (DIRECT-Protect 2): a randomised placebo-controlled trial. Lancet 2008;372:1385–93. PMID: 18823658.
  7. Reaven PD, Emanuelle N, Moritz T et al. Proliferative diabetic retinopathy in type 2 patients is related to coronary artery calcium in the Veterans Affairs Diabetes Trial (VADT). Diabetes Care 2008;31:952–7. PMID: 18316393.
  8. Al-Ansari SA, Tennant MT, Freve MD, Hinz BJ, Senior PA. Short report: sub-optimal diabetes care in high-risk diabetic patients attending a specialist retina clinic. Diabetic Med 2009;26:1296–300. PMID: 20002485.
  9. Shah AS, Chen SH. Cataract surgery and diabetes. Curr Opin Ophthalmol 2010;21:4–9. PMID: 19935423.


For more information and to purchase this book, just follow this link:


David Levy, MD, FRCP, Consultant Physician, Gillian Hanson Centre, Whipps Cross University Hospital; Honorary Senior Lecturer
Queen Mary University of London London, UK

This edition first published 2011, © 2011 by David Levy. 1st edition 1998 (Greenwich Medical Media/Cambridge University Press) 2nd edition 2006 (Altman Publications)